These results prompted us to conduct a similar analysis of our ALIAS Pilot Trial data, in the 42 subjects in whom plasma BNP levels were measured.2 Spearman rank-order correlation analysis revealed no significant relationship between baseline hematocrit and baseline BNP level (ρ=−0.272, P=0.081); no relationship between 24-hour (post-ALB treatment) hematocrit and post-ALB BNP level (ρ=−0.011, P=0.95); and no relationship between the ALB-induced decrease in hematocrit and increase in BNP level at 24 hours after ALB treatment (ρ=−0.051, P=0.76).

We also conducted a multiple linear regression analysis incorporating both age and hematocrit level. Both initial and 24-hour BNP levels were highly correlated to the subjects’ age (P<0.001) but were not correlated to the corresponding hematocrit value (P=0.31 and 0.17, respectively). Similarly, the rise in BNP at 24 hours was highly correlated to age (P<0.001) but not to the change in hematocrit (P=0.6). A regression plot of the latter data is shown below (Figure).

Increase in plasma BNP level from baseline to 24 hours post-treatment, plotted as a function of the decrease in hematocrit from baseline to 24 hours post-treatment, in individual subjects of the ALIAS Pilot Trial who received 25% human albumin at doses ranging from 1.37 to 2.05 g/kg body weight.2

Thus, we are unable to confirm the conclusions of Drs Muscari and Zoli. It should be noted that, whereas they assessed the BNP precursor, we assayed BNP itself. This might have some bearing on the discrepancy.